BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in acute myeloid leukemia.

Activating mutations of KIT play an important role in the pathophysiology of several human malignancies, including acute myeloid leukemia.

Here we examined the potency of a novel KIT inhibitor KI-328 against different types of mutant KIT kinases recurrently identified in AML.

Furthermore, HSP90 inhibitors suppress the growth of D816V-KIT-expressing cells at the concentration at which the growth of other mutant-KIT-expressing cells is not affected.

[MeSH-major] Antineoplastic Agents / pharmacology. Carbamates / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology

[MeSH-minor] Cell Line, Tumor. Humans. K562 Cells

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Bioorg Med Chem Lett. 2008 Oct 15;18(20):5472-7 [18835166.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]

[Cites] Blood. 2002 Mar 1;99(5):1741-4 [11861291.001]

[Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]

[Cites] Cell. 1991 Jun 28;65(7):1143-52 [1648448.001]

[Cites] Br J Dermatol. 2008 Nov;159(5):1160-9 [18795925.001]

[Cites] Blood. 2009 Aug 20;114(8):1607-17 [19541823.001]

[Cites] Br J Haematol. 2007 Jul;138(1):12-30 [17555444.001]

[Cites] Blood. 2004 Feb 1;103(3):1078-84 [14551138.001]

[Cites] Leukemia. 2009 Jan;23(1):95-103 [18830255.001]

[Cites] Clin Cancer Res. 2009 Jan 1;15(1):9-14 [19118027.001]

[Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]

[Cites] Leukemia. 2000 Mar;14(3):374-8 [10720129.001]

[Cites] Eur J Haematol. 2009 Aug;83(2):90-8 [19309322.001]

[Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]

[Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]

[Cites] J Biol Chem. 2008 Jul 4;283(27):18473-7 [18442971.001]

[Cites] EMBO J. 1987 Nov;6(11):3341-51 [2448137.001]

[Cites] J Clin Oncol. 2005 Sep 10;23(26):6285-95 [16155011.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):473-81 [16397263.001]

[Cites] Cancer Res. 2006 Sep 15;66(18):9153-61 [16982758.001]

[Cites] Blood. 2007 Jan 1;109(1):315-22 [16912224.001]

[Cites] Blood. 2004 Dec 1;104(12):3754-7 [15304388.001]

[Cites] Leukemia. 2002 Aug;16(8):1535-40 [12145695.001]

[Cites] Science. 1998 Jan 23;279(5350):577-80 [9438854.001]

[Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]

[Cites] Mol Cancer Ther. 2003 May;2(5):471-8 [12748309.001]

[Cites] Cancer Cell. 2003 Mar;3(3):213-7 [12676580.001]

[Cites] Proc Natl Acad Sci U S A. 2009 Feb 3;106(5):1542-7 [19164557.001]

[Cites] Blood. 1997 Aug 15;90(4):1345-64 [9269751.001]

[Cites] Lancet Oncol. 2005 Apr;6(4):249-51 [15811621.001]

[Cites] Biochem Biophys Res Commun. 2005 Dec 23;338(3):1307-15 [16226710.001]

[Cites] Blood. 2006 Mar 1;107(5):1791-9 [16254134.001]

[Cites] Blood. 2005 Oct 15;106(8):2865-70 [15972446.001]

[Cites] J Biol Chem. 2003 Aug 22;278(34):31461-4 [12824176.001]

[Cites] Mol Cancer Ther. 2002 Oct;1(12):1115-24 [12481435.001]

[Cites] J Clin Oncol. 2002 Mar 15;20(6):1692-703 [11896121.001]

[Cites] J Clin Invest. 1993 Oct;92(4):1736-44 [7691885.001]

[Cites] Br J Cancer. 2009 May 19;100(10):1523-9 [19401686.001]

[Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4575-82 [17671144.001]

[Cites] PLoS One. 2009 Sep 30;4(9):e7258 [19789626.001]

[Cites] Blood. 1991 Dec 1;78(11):2962-8 [1720040.001]

[Cites] Stem Cells. 2005;23(1):16-43 [15625120.001]

(PMID = 20890793.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / HSP90 Heat-Shock Proteins; 0 / KI 328; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Myeloid sarcoma of the prostate revealed by urinary retention: a case report.

Myeloid sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.

Here, a singular case of a MS of the prostate discovered through investigations for urinary retention and revealing an acute leukaemia classified as an acute myeloid leukaemia (AML) with inversion 16 (inv16) according to the World Health Organization (WHO) classification (AML-M4 with inv16 in the French-American-British (FAB) classification) in a 65-year-old man is presented.

None of the previously reported and reviewed cases of prostatic MS were of AML-M4 type.

Such a translocation was recently described in some acute myeloid processes.

Radiation therapy could be beneficial for the localised disease of the prostate.

Allogenic haematopoietic stem cell transplantation is also a promising therapy for MS.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Haematologica. 1953;37(8):827-34 [13128526.001]

[Cites] Br J Surg. 1960 May;47:658-60 [13838365.001]

[Cites] Ann Hematol. 2004 Feb;83(2):78-83 [14551738.001]

[Cites] Lancet Oncol. 2004 Jan;5(1):62-3 [14700611.001]

[Cites] Cancer. 2006 Nov 1;107(9):2099-107 [17019734.001]

[Cites] Leuk Lymphoma. 2006 Dec;47(12):2527-41 [17169797.001]

[Cites] J Urol. 1947 Oct;58(4):272-6 [20266242.001]

[Cites] Ann Hematol. 1994 Feb;68(2):97-9 [8148423.001]

[Cites] Prog Urol. 1998 Sep;8(4):569-72 [9834524.001]

[Cites] Int Urol Nephrol. 2004;36(1):55-6 [15338675.001]

[Cites] Urol Oncol. 2005 Nov-Dec;23(6):419-21 [16301120.001]

[Cites] Br J Urol. 1990 Jun;65(6):655-6 [2372683.001]

[Cites] Cancer. 1987 Jan 1;59(1):142-6 [2431755.001]

[Cites] Cancer. 1970 Dec;26(6):1361-5 [4098491.001]

[Cites] G Gerontol. 1967 May;15(5):605-14 [5250187.001]

[Cites] Cancer. 1983 Jun 15;51(12):2164-7 [6573938.001]

[Cites] Am J Hematol. 1996 Dec;53(4):267-71 [8948669.001]

(PMID = 21686890.001).

[ISSN] 1757-790X

[Journal-full-title] BMJ case reports

[ISO-abbreviation] BMJ Case Rep

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC3029613

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in acute myeloid leukemia.

Tryptases are predominantly mast cell-specific serine proteases with pleiotropic biological activities.

Recently, significant amounts of tryptases have been shown to be produced by myeloblasts in certain patients with acute myeloid leukemia (AML), but the function of secreted tryptases in pathological circumstances remains unknown.

In this study, we investigated whether beta-tryptase affects the expression of vascular endothelial growth factor (VEGF) in bone marrow stromal cells (BMSCs) in AML.

We detected the expression of proteinase-activated receptor-2 (PAR-2) on AML BMSCs and found that beta-tryptase significantly up-regulated VEGF mRNA and protein expression in a dose-dependent manner by real-time PCR, Western blot, and ELISA.

These results suggest that beta-tryptase up-regulates VEGF production in AML BMSCs via the PAR-2, ERK1/2, and p38MAPK signaling pathways.

[MeSH-major] Bone Marrow Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Mitogen-Activated Protein Kinases / metabolism. Receptor, PAR-2 / metabolism. Stromal Cells / metabolism. Tryptases / metabolism. Vascular Endothelial Growth Factor A / metabolism

[MeSH-minor] Blotting, Western. Cell Proliferation. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoenzyme Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20578818.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.59 / Tryptases

   

Advertisement

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.

DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology.

Its impact in leukemia progression is not fully understood.

We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.

We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with AML, both at diagnosis and relapse.

Abnormal methylation was found in 23% to 83% of patients at diagnosis and in 47% to 93% at relapse, with CDH13 being the most frequently methylated.

We observed concordance in methylation of several genes, confirming the presence of a hypermethylator pathway in AML.

DNA methylation levels increased at relapse in 25 of 30 (83%) patients with AML.

These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at diagnosis and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001).

Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 2001 May 1;97(9):2823-9 [11313277.001]

[Cites] Cancer Res. 2007 Mar 1;67(5):1997-2005 [17332327.001]

[Cites] Blood. 2002 Oct 15;100(8):2957-64 [12351408.001]

[Cites] J Clin Oncol. 2003 Apr 15;21(8):1472-9 [12697869.001]

[Cites] Blood. 2003 May 15;101(10):4131-6 [12586619.001]

[Cites] Biotechniques. 2003 Jul;35(1):146-50 [12866414.001]

[Cites] Clin Cancer Res. 2003 Aug 1;9(8):2879-81 [12912930.001]

[Cites] Nucleic Acids Res. 2004;32(3):e38 [14973332.001]

[Cites] Cancer Res. 2004 Apr 1;64(7):2411-7 [15059893.001]

[Cites] FEBS Lett. 2004 Jun 4;567(2-3):327-32 [15178346.001]

[Cites] Nucleic Acids Res. 1994 Aug 11;22(15):2990-7 [8065911.001]

[Cites] Cancer Res. 1996 Feb 15;56(4):722-7 [8631003.001]

[Cites] Cancer Res. 1996 Mar 1;56(5):973-77 [8640788.001]

[Cites] J Mol Biol. 1996 Nov 29;264(2):268-78 [8951376.001]

[Cites] Cancer Res. 1999 May 15;59(10):2307-12 [10344734.001]

[Cites] Cancer Res. 1999 Jul 15;59(14):3352-6 [10416592.001]

[Cites] Nat Rev Cancer. 2004 Dec;4(12):988-93 [15573120.001]

[Cites] Nat Genet. 2005 Mar;37(3):265-74 [15723065.001]

[Cites] Br J Cancer. 2005 Mar 28;92(6):1165-72 [15756280.001]

[Cites] J Clin Oncol. 2005 Jun 10;23(17):3948-56 [15883410.001]

[Cites] Mol Cancer Res. 2005 Jun;3(6):325-34 [15972851.001]

[Cites] J Clin Oncol. 2005 Sep 10;23(26):6285-95 [16155011.001]

[Cites] J Clin Oncol. 2005 Oct 1;23(28):7043-9 [16192589.001]

[Cites] Semin Oncol. 2005 Oct;32(5):521-30 [16210093.001]

[Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]

[Cites] Ann Hematol. 2005 Dec;84 Suppl 1:39-46 [16231140.001]

[Cites] Br J Haematol. 2006 May;133(3):276-83 [16643429.001]

[Cites] Cancer Res. 2006 May 15;66(10):5077-84 [16707430.001]

[Cites] Clin Cancer Res. 2006 Aug 15;12(16):4845-50 [16914570.001]

[Cites] Br J Cancer. 2006 Oct 23;95(8):1108-13 [17047656.001]

[Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]

[Cites] Cancer Res. 2007 Feb 1;67(3):876-80 [17283117.001]

[Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]

[Cites] Blood. 2007 May 1;109(9):3895-905 [17234736.001]

[Cites] Genome Res. 2007 Oct;17(10):1529-36 [17785535.001]

[Cites] PLoS Genet. 2007 Oct;3(10):2023-36 [17967063.001]

[Cites] Oncogene. 2002 Apr 18;21(17):2741-9 [11965547.001]

(PMID = 18523155.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ PMC2515110

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Glutathione S-transferase A1 polymorphisms and acute graft-vs.-host disease in HLA-matched sibling allogeneic hematopoietic stem cell transplantation.

We assessed whether the clinical outcomes, including acute graft-vs.-host disease, of 61 patients with hematological malignancies, following HLA-matched sibling allogeneic stem cell transplantation using busulfan/cyclophosphamide conditioning are altered by glutathione S-transferase A1 genotypes.

Globally, grade II-IV acute graft-vs.-host disease developed in 13 patients (21%).

Grade II-IV acute graft-vs.-host disease developed in 15.2% of 46 patients with GSTA1*A/*A diplotype and in 40.0% of 15 patients with GSTA1*A/*B or GSTA1*B/*B diplotype (p = 0.04).

Moreover, this relationship between GSTA1*A/*A diplotypes and lower incidence of acute graft-vs.-host disease was independent of the age, gender, stem cell source, and disease status.

The incidences of acute skin graft-vs.-host disease were 7% (3/46) in patients with GSTA1*A/*A and 27% (4/15) in patients without GSTA1*A/*A (p = 0.009, univariate; p = 0.01, multivariate).

Acute hepatic graft-vs.-host disease developed in 6 (13%) of 46 patients with the GSTA1*A/*A diplotype and in 4 (27%) of 15 patients without this diplotype (p = 0.09, univariate; p = 0.12, multivariate).

Ten patients (16%) developed hepatic veno-occlusive disease.

No significant difference was found in the incidence of hepatic veno-occlusive disease between patients with and without the GSTA1*A/*A diplotype (19.6% vs. 6.7%; p = 0.24).

We conclude that the GSTA1*A/*A diplotype is an independent protective factor against acute graft-vs.-host disease, especially for skin graft-vs.-host disease, and probably for hepatic graft-vs.-host disease, in patients using busulfan/cyclophosphamide conditioning.

The identification of glutathione S-transferase A1 genotypes prior to allogeneic stem cell transplantation could allow conditioning regimens and graft-vs.-host disease prophylaxis to be modified to improve outcome.

[MeSH-major] Glutathione Transferase / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation. Polymorphism, Single Nucleotide

[MeSH-minor] Acute Disease. Adult. Female. Genotype. Hepatic Veno-Occlusive Disease / etiology. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid / surgery. Male. Middle Aged. Siblings. Transplantation Conditioning

Genetic Alliance. consumer health - Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17425746.001).

[ISSN] 0902-0063

[Journal-full-title] Clinical transplantation

[ISO-abbreviation] Clin Transplant

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] EC 2.5.1.18 / GSTA1 protein, human; EC 2.5.1.18 / Glutathione Transferase

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.

Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM area (LMA), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.

Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with LMA.

Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with LMA (0.32).

The genetic correlation between LMA and DL was positive and high (0.64).

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16100060.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9007-34-5 / Collagen

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Allogeneic stem cell transplantation in children with leukemia using human leukocyte antigen-mismatched unrelated donors.

Allogeneic HSCT is a curative treatment, when chemotherapy fails, for certain malignant diseases.

We present our data of HSCT using HLA partially allele-mismatched (7-8/10) UDs in 24 children with leukemia.

Acute GvHD grade II was diagnosed in 70.8% of the patients and grade III-IV in 12.5%.

It enables stable engraftment, good control of GvHD, full reconstitution of immunity, and is not connected with unacceptable transplant-related mortality.

[MeSH-major] Graft vs Host Disease / prevention & control. Leukemia / surgery. Stem Cell Transplantation

[MeSH-minor] Adolescent. Antilymphocyte Serum / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Male. Tissue Donors. Transplantation Immunology

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18186885.001).

[ISSN] 1397-3142

[Journal-full-title] Pediatric transplantation

[ISO-abbreviation] Pediatr Transplant

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Antilymphocyte Serum

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.

Traditionally, patients with acute leukaemia are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.

We have developed an outpatient treatment programme for patients with acute leukaemia incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).

Herein, we report the results of outpatient treatment of 60 patients with acute leukaemia (54 with acute myeloid leukaemia) followed prospectively in the period from March 2004 to 2007.

We conclude that outpatient treatment of patients with acute leukaemia is feasible and safe.

[MeSH-major] Ambulatory Care / methods. Anti-Infective Agents / administration & dosage. Leukemia / drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20002732.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.

Acute myeloid leukemia (AML) remains the most common form of leukemia and the most common cause of leukemia death.

Although conventional chemotherapy can cure between 25 and 45% of AML patients, the majority of patients die after relapse or of complications associated with treatment.

Thus, more specific and less toxic treatments for AML patients are needed, especially for elderly patients.

An indispensable prerequisite to investigate tailored approaches for AML is the recent progress in the understanding the molecular features that distinguish leukemia progenitors from normal hematopoietic counterparts and the identification of a variety of dysregulated molecular pathways.

In this review, we describe some of the signaling pathways that are aberrantly regulated in AML, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects

[MeSH-minor] Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to Disease / genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18534059.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases

[Number-of-references] 126

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Patients with neutropenia resulting from chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome are at high risk for difficult-to-treat and often fatal invasive fungal infections.

CONCLUSIONS: In patients undergoing chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome, posaconazole prevented invasive fungal infections more effectively than did either fluconazole or itraconazole and improved overall survival.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Male. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / mortality. Single-Blind Method. Treatment Outcome

MedlinePlus Health Information. consumer health - Fungal Infections.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827852315 for PMID:17251531 [PharmGKB] .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

Hazardous Substances Data Bank. Itraconazole .

Hazardous Substances Data Bank. FLUCONAZOLE .

SciCrunch. DrugBank: Data: Chemical .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2007 Massachusetts Medical Society.

[CommentIn] Nat Clin Pract Oncol. 2007 Sep;4(9):512-3 [17646862.001]

[CommentIn] Curr Infect Dis Rep. 2007 Nov;9(6):446-7 [17999879.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2215; author reply 2215-8 [17526089.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2214-5; author reply 2215-8 [17526090.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2214; author reply 2215-8 [17522407.001]

[CommentIn] N Engl J Med. 2007 Jan 25;356(4):409-11 [17251538.001]

(PMID = 17251531.001).

[ISSN] 1533-4406

[Journal-full-title] The New England journal of medicine

[ISO-abbreviation] N. Engl. J. Med.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00044486

[Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 8VZV102JFY / Fluconazole

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.

This is the first study of FLT3 mutations in pediatric non-promyelocytic AML patients that received the same treatment scheme in single institute.

Patients with FLT3/TKD remain alive after autologous stem cell transplantation.

The disease-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).

New therapeutic scheme such as stem cell transplantation with more intensive conditioning just after complete remission could be applied in pediatric non-promyelocytic AML patients with the FLT3/ITD mutation.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15863200.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Feverfew: weeding out the root of leukaemia.

Malignant stem cells are central to the pathogenesis and perpetuation of acute myelogenous leukaemia (AML).

Despite their crucial role, standard chemotherapy often does not target these critical cells and, thus, the 'root' of leukaemic disease is not eradicated.

To derive better therapies, unique molecular features of malignant stem cells have been characterised for AML and evaluated with regard to ablation of disease.

In the course of such studies, the compound parthenolide, which is derived from the medicinal plant feverfew, has recently been shown to preferentially induce AML stem cells to undergo apoptosis.

Thus, this naturally occurring agent may provide new avenues of investigation for the treatment of leukaemia.

[MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Neoplastic Stem Cells / drug effects. Sesquiterpenes / pharmacology. Tanacetum parthenium / chemistry

[MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Humans. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Plants, Medicinal / chemistry. Xenograft Model Antitumor Assays

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16120045.001).

[ISSN] 1744-7682

[Journal-full-title] Expert opinion on biological therapy

[ISO-abbreviation] Expert Opin Biol Ther

[Language] eng

[Publication-type] Editorial

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.

Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).

So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.

In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).

Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.

[MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Platelet Disorders.

SciCrunch. OMIM: Data: Gene Annotation .

SciCrunch. Clinical Genomic Database: Data: Gene Annotation .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19357396.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.

The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).

JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with myelodysplastic syndromes.

No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or acute lymphoblastic leukemia (20 patients).

We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the acute phase of these diseases and that it is generally rare in aggressive leukemias.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Anal Biochem. 2000 Apr 10;280(1):103-10 [10805527.001]

[Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]

[Cites] Cancer. 2002 Oct 15;95(8):1673-84 [12365015.001]

[Cites] Arch Pathol Lab Med. 2003 May;127(5):601-5 [12708906.001]

[Cites] Cell. 1993 Jul 30;74(2):227-36 [8343951.001]

[Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]

[Cites] Cell. 1998 May 1;93(3):385-95 [9590173.001]

[Cites] Blood. 2005 Feb 1;105(3):973-7 [15388582.001]

[Cites] Curr Opin Hematol. 2005 Mar;12(2):112-6 [15725900.001]

[Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]

[Cites] J Clin Oncol. 2005 Apr 1;23(10):2224-32 [15710945.001]

[Cites] Cancer Res. 2005 Apr 1;65(7):2662-7 [15805263.001]

[Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]

[Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]

[Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]

[Cites] J Biol Chem. 2005 Jun 17;280(24):22788-92 [15863514.001]

[Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]

[Cites] Blood. 2002 Feb 1;99(3):840-9 [11806985.001]

(PMID = 16037387.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50CA100632

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2

[Other-IDs] NLM/ PMC1895065

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Optimizing the classification of acute lymphoblastic leukemia and acute myeloid leukemia samples using artificial neural networks.

Accurate classification of human blood cells plays a decisive role in the diagnosis and treatment of diseases.

Artificial Neural Networks (ANN) have been consistently used as a trusted classification tool for this type of analysis.

In this study, a new Artificial Neural Network approach is proposed for the multidimensional classification of two of the most common forms of leukemia: Acute Lymphoblastic Leukemia (ALL) and Acute Myeloid Leukemia (AML), also sometimes called Acute Myelogenous Leukemia.

The goal was to establish a programming tool, supported through this new ANN development, for the identification of normal and abnormal blood samples and provide information to medical doctors in the form of diagnostic references for the specific disease state that is considered for this study.

The application of the ANN algorithm produced remarkable classification accuracy results that show a 95% classification accuracy for the normal blood samples and 90% classification accuracy for the abnormal samples even under the ubiquitous problem of overlap.

[MeSH-major] Blood Cell Count / methods. Diagnosis, Computer-Assisted / methods. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Neural Networks (Computer). Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Blood Cells / classification. Cluster Analysis. Humans. Pattern Recognition, Automated / methods. Quality Control. Reproducibility of Results. Sensitivity and Specificity

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Blood Count Tests.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16817618.001).

[ISSN] 0067-8856

[Journal-full-title] Biomedical sciences instrumentation

[ISO-abbreviation] Biomed Sci Instrum

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Is age an independent risk factor for chemically induced acute myelogenous leukemia in children?

Secondary or therapy-related acute myelogenous leukemia (t-AML) is a rare but unfortunate consequence of treatment with certain classes of cytotoxic chemotherapeutic agents or chronic exposure to high concentrations of benzene.

Drugs known to produce AML following chemotherapy of primary malignancy are usually alkylating agents or topoisomerase II inhibitors.

Both children and adults develop AML following treatment with these classes of antineoplastic drugs.

In this review, the effect of age at treatment on a child's susceptibility to developing therapy related AML was investigated.

As demonstrated in the published literature, the risk of developing AML following chemotherapy is not reliably correlated with the age of the pediatric patient.

For example, secondary solid tumors such as breast, central nervous system (CNS), bone, and thyroid cancer are highly dependent on the age of the patient at time of diagnosis and treatment; in contrast, an age dependency for t-AML risk was not observed in these same patient populations.

Predictably, the induction of t-AML in children follows a rational dose-response relationship, with increasing doses of chemotherapy resulting in greater risk. Recent U.S.

Available scientific and medical literature does not support the hypothesis that children necessarily possess an increased risk of developing AML following leukemogenic chemical exposure.

[MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Neoplasms, Second Primary / epidemiology

[MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease Susceptibility. Humans. Risk Factors. Topoisomerase II Inhibitors

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17687725.001).

[ISSN] 1521-6950

[Journal-full-title] Journal of toxicology and environmental health. Part B, Critical reviews

[ISO-abbreviation] J Toxicol Environ Health B Crit Rev

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors

[Number-of-references] 92

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.

Myeloid sarcoma (MS) is a rare extramedullary malignant tumor composed of immature myeloid cells.

It is strongly associated with a well known or covert acute myeloid leukaemia, chronic myeloproliferative diseases or myelodysplastic syndromes.

An unusual case of acute myeloid leukaemia, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.

The histological examination (including immunohistochemical analysis) of a subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.

This lesion was therefore classified as acute myeloid leukaemia.

The patient was referred to oncologists that confirmed the initial diagnosis.

Forty days later, a relapse of the disease, which appeared as a great-ulcerated lesion, was developed in the hard palate.

Review of the literature shows no report of intraoral relapse and particularly multiple relapse of a MS that involves the oral cavity.

Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential diagnosis of conditions (especially tumors) with a similar clinical appearance.

[MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Sarcoma, Myeloid / diagnosis

[MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Diagnosis, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms

Genetic Alliance. consumer health - Myeloid sarcoma.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. ETOPOSIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Oral Maxillofac Surg. 1990 Jul;48(7):748-52 [2193130.001]

[Cites] Leuk Res. 2004 Jan;28(1):25-34 [14630077.001]

[Cites] J Periodontol. 2003 Oct;74(10):1514-9 [14653399.001]

[Cites] Quintessence Int. 2007 Nov-Dec;38(10):817-20 [18197320.001]

[Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Jan;105(1):e34-6 [18155599.001]

[Cites] Isr Med Assoc J. 2003 Jun;5(6):452 [12841024.001]

[Cites] Oral Oncol. 2002 Jul;38(5):516-9 [12110349.001]

[Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001 Dec;92(6):689-93 [11740487.001]

[Cites] Oral Oncol. 2000 Sep;36(5):491-4 [10964059.001]

[Cites] Int J Hematol. 2005 Feb;81(2):138-41 [15765782.001]

[Cites] J Oral Maxillofac Surg. 1991 Dec;49(12):1346-50 [1955927.001]

[Cites] Pediatr Blood Cancer. 2007 Apr;48(4):393-8 [16550530.001]

[Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 Jun;103(6):e44-8 [17428693.001]

(PMID = 20512638.001).

[ISSN] 1936-0568

[Journal-full-title] Head and neck pathology

[ISO-abbreviation] Head Neck Pathol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide

[Other-IDs] NLM/ PMC2878628

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.

BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most acute myeloid leukemias (AMLs).

Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype AMLs and are an independent predictor of poor outcome in this subgroup of patients with AML.

METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with AML who were treated on the Acute Leukemia French Association 9802 trial.

Within the subgroup of patients who had normal karyotype AML (n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.

CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with AML.

Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with AML.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19536888.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.

The mechanisms underlying deregulation of HOX gene expression in AML are poorly understood.

Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause acute myeloid leukemia (AML) in mice.

In contrast inactivation of the putative Pbx interacting site of Cdx2 did not change the leukemogenic potential of the gene.

In an analysis of 115 patients with AML, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.

All patients with AML with normal karyotype tested were negative for CDX1 and CDX4 expression.

They furthermore correlate the level of CDX2 expression with HOX gene expression in human AML and support a potential role of CDX2 in the development of human AML with aberrant Hox gene expression.

[MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics

[MeSH-minor] Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation. Cell Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17855634.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].

OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.

METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.

RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.

The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.

21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.

21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.

17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.

CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.

21) (q22; q22)/AML-ETO fusion gene and t (15;.

[MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16321221.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (LMAs).

The cuffs of both ETTs and LMAs inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).

METHODS: The change in dimensions of the inflated cuffs of a size 8 ETT and a size 5 LMA were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.

RESULTS: A linear expansion in cuff dimensions as a function of altitude increase was identified.

CONCLUSION: The data for LMA cuff expansion failed to show significant correlation with altitude change.

Further work is required to determine a similar rule of thumb for LMA cuff deflation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Anaesthesia. 2000 Dec;55(12):1179-84 [11121927.001]

[Cites] Anaesthesia. 2002 Apr;57(4):374-8 [11939997.001]

[Cites] Anaesthesia. 2004 Mar;59(3):252-4 [14984523.001]

[Cites] Anaesthesia. 1975 Jan;30(1):4-11 [1115341.001]

[Cites] Br Med J (Clin Res Ed). 1984 Mar 31;288(6422):965-8 [6423162.001]

[Cites] J Trauma. 1999 Aug;47(2):352-7 [10452473.001]

[CommentIn] Emerg Med J. 2007 Aug;24(8):605 [17652705.001]

(PMID = 17351218.001).

[ISSN] 1472-0213

[Journal-full-title] Emergency medicine journal : EMJ

[ISO-abbreviation] Emerg Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2660019

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.

We report the case of a child affected by acute myeloid leukaemia who was treated with allogeneic haematopoietic stem cell transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.

The diagnosis was difficult on a clinical basis, but made possible by conventional radiography and MRI.

[MeSH-major] Aspergillosis / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal Diseases / microbiology

[MeSH-minor] Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage. Diagnosis, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant. Leukemia, Myeloid, Acute / surgery. Magnetic Resonance Imaging. Male. Radiography. Rare Diseases. Recurrence. Spine / diagnostic imaging. Spine / pathology

Genetic Alliance. consumer health - Osteomyelitis.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Aspergillosis.

MedlinePlus Health Information. consumer health - Spine Injuries and Disorders.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Pediatr Radiol. 2003 Jul;33(7):453-60 [12739082.001]

[Cites] Clin Infect Dis. 1998 Apr;26(4):781-803; quiz 804-5 [9564455.001]

[Cites] J Infect. 2000 Jul;41(1):97-100 [11041713.001]

[Cites] Blood. 2002 Dec 15;100(13):4358-66 [12393425.001]

[Cites] Acta Orthop Belg. 1993;59(3):306-14 [8237349.001]

[Cites] Pediatrics. 1994 May;93(5):830-5 [8165091.001]

[Cites] Pediatr Neurosurg. 2001 Jul;35(1):18-23 [11490186.001]

[Cites] Clin Infect Dis. 2001 Jan;32(1):9-16 [11112668.001]

(PMID = 18392819.001).

[ISSN] 0301-0449

[Journal-full-title] Pediatric radiology

[ISO-abbreviation] Pediatr Radiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Drug delivery in acute myeloid leukemia.

BACKGROUND: Acute myeloid leukemia was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.

OBJECTIVE: We have chosen acute myeloid leukemia as a disease prototype to review established and novel targeted approaches in leukemia treatment.

CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation for leukemia-directed uptake, their efficacy has probably not changed significantly.

Further improvements may result from the characterization of novel acute myeloid leukemia (AML) cell surface receptors and of leukemic stem cells, as well as from the design of leukemia-targeted gene therapy vectors.

[MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3

Genetic Alliance. consumer health - Leukemia, Myeloid.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18532921.001).

[ISSN] 1742-5247

[Journal-full-title] Expert opinion on drug delivery

[ISO-abbreviation] Expert Opin Drug Deliv

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3

[Number-of-references] 114

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.

EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of acute myeloid leukemia (AML) patients.

RESULTS: The antibody did not impair the growth of MOLT-4 and U-937 cells in culture.

Its conjugate with curcumin, however, was lethal to both cell lines.

The immunoconjugate killed tumor cells bearing the CD33 marker of an AML patient expressing hCGbeta but did not have a similar action on cells of another AML patient with the CD13 marker but who was negative for hCGbeta.

[MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism. Leukemia / drug therapy. Lymphoma / drug therapy

[MeSH-minor] Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Separation. Drug Design. Female. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells

MedlinePlus Health Information. consumer health - Leukemia.

MedlinePlus Health Information. consumer health - Lymphoma.

Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .

Hazardous Substances Data Bank. CURCUMIN .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19127081.001).

[ISSN] 1423-0232

[Journal-full-title] Oncology

[ISO-abbreviation] Oncology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The majority of malignancies were distributed equally between T and B cell neoplasms and included lymphoblastic T cell lymphoma (LTCL), lymphoblastic B cell lymphoma (LBCL), diffuse large B cell lymphoma (DLBCL), the histiocyte/T cell rich variant of DLBCL (DLBCL-HA/T cell rich DLBCL), splenic marginal zone lymphoma (SMZL), follicular B cell lymphoma (FBL) and plasmacytoma (PCT).

Most of these neoplasms were highly similar to human diseases.

Also, some non-lymphoid malignancies such as acute myeloid leukemia (AML) and histiocytic sarcoma were found.

Interestingly, composite lymphomas, including Hodgkin-like lymphomas, were also detected that had CD30(+) Hodgkin/Reed-Sternberg (H/RS)-like cells, representing a tumor type not previously described in mice.

Thus, this DR4 line is a useful model to investigate common molecular mechanisms that may contribute to important neoplastic diseases in man.

[MeSH-major] Chimerism. Hematologic Neoplasms / immunology. Hematologic Neoplasms / pathology. Histocompatibility Antigens Class II / immunology. Hodgkin Disease / immunology. Hodgkin Disease / pathology

[MeSH-minor] Animals. Antigens, CD30 / metabolism. Base Sequence. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology. Mice. Mice, Transgenic. Molecular Sequence Data. Reed-Sternberg Cells / pathology. Survival Analysis. Transgenes / genetics

MedlinePlus Health Information. consumer health - Hodgkin Disease.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]

[Cites] Diagn Mol Pathol. 2002 Mar;11(1):2-8 [11854595.001]

[Cites] Oncogene. 2002 Sep 26;21(43):6559-66 [12242653.001]

[Cites] Am J Surg Pathol. 2002 Nov;26(11):1458-66 [12409722.001]

[Cites] Blood. 2003 Feb 15;101(4):1505-12 [12393731.001]

[Cites] Am J Surg Pathol. 2003 Dec;27(12):1577-80 [14657719.001]

[Cites] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W435-40 [15215425.001]

[Cites] Methods Cell Biol. 1989;30:353-77 [2494418.001]

[Cites] Int J Cancer. 1992 Dec 2;52(6):887-91 [1459730.001]

[Cites] J Exp Med. 1993 May 1;177(5):1257-68 [8386741.001]

[Cites] Proc Natl Acad Sci U S A. 1993 May 1;90(9):4319-23 [8483950.001]

[Cites] Blood. 1993 Aug 15;82(4):1247-56 [8353287.001]

[Cites] J Exp Med. 1995 Apr 1;181(4):1587-91 [7699339.001]

[Cites] Annu Rev Immunol. 1995;13:417-35 [7612230.001]

[Cites] Eur J Immunol. 1995 Oct;25(10):2813-7 [7589076.001]

[Cites] J Exp Med. 1996 Jun 1;183(6):2635-44 [8676084.001]

[Cites] Ann Oncol. 1996;7 Suppl 4:27-30 [8836405.001]

[Cites] J Exp Med. 1996 Oct 1;184(4):1495-505 [8879220.001]

[Cites] N Engl J Med. 1999 Apr 22;340(16):1239-47 [10210707.001]

[Cites] Exp Hematol. 1999 Apr;27(4):682-8 [10210326.001]

[Cites] Histopathology. 2005 Feb;46(2):217-28 [15693895.001]

[Cites] Cancer Res. 2005 Feb 15;65(4):1306-15 [15735016.001]

[Cites] Mutat Res. 2005 Jul 1;574(1-2):3-21 [15914203.001]

[Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]

[Cites] Exp Toxicol Pathol. 2006 Jul;57(5-6):377-81 [16713211.001]

[Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1213-24 [16815105.001]

[Cites] Pathol Biol (Paris). 2007 Feb;55(1):73-83 [16815642.001]

[Cites] Cell Cycle. 2007 Mar 1;6(5):543-5 [17329976.001]

[Cites] Toxicol Pathol. 2007 Apr;35(3):366-75 [17455084.001]

[Cites] Curr Protoc Hum Genet. 2001 May;Chapter 4:Unit4.10 [18428279.001]

[Cites] Immunol Rev. 1999 Dec;172:335-43 [10631958.001]

[Cites] Leukemia. 2000 Jul;14(7):1174-84 [10914539.001]

[Cites] Nucleic Acids Res. 2001 Jan 1;29(1):207-9 [11125093.001]

[Cites] Cytometry. 2001 Feb 1;43(2):101-9 [11169574.001]

[Cites] Blood. 2002 Jul 1;100(1):246-58 [12070034.001]

(PMID = 20046882.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD30; 0 / Histocompatibility Antigens Class II

[Other-IDs] NLM/ PMC2796171

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.

Achyrocline satureioides (LAM.

They were isolated from 18 patients with acne lesions and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).

On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control non-infected individuals.

The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the lymphocyte expansion, of which 40% were CD8+ T cells.

[MeSH-minor] Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans. Lymphocyte Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology

MedlinePlus Health Information. consumer health - Antibiotics.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18293658.001).

[ISSN] 0187-4640

[Journal-full-title] Revista latinoamericana de microbiología

[ISO-abbreviation] Rev. Latinoam. Microbiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Mexico

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.

The volatile components of the flowerheads of Centaurea eryngioides Lam. and Centaurea iberica Trev. var. hermonis Boiss. Lam. were obtained by hydrodistillation and identified by GC and GC-MS.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16317829.001).

[ISSN] 1478-6419

[Journal-full-title] Natural product research

[ISO-abbreviation] Nat. Prod. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Oils, Volatile; 0 / Plant Oils

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis.

BACKGROUND: Nucleophosmin (NPM1) gene mutations are reported to predict a favorable prognosis in acute myeloid leukemia (AML) patients.

RESULTS: The study included 252 AML patients: 192 de novo AML, 33 AML preceded by either myelodysplastic syndrome or chronic myelomonocytic leukemia, and 27 therapy-related AML.

Cytoplasmic NPM was detected in 59 of 252 (23%) patients, including 48 of 192 (25%) de novo AML and 33 of 94 (35%) with a normal karyotype.

CONCLUSIONS: IHC assessment for NPM localization did not predict prognosis in this patient cohort.

[MeSH-major] Bone Marrow / metabolism. Cytoplasm / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2009 American Cancer Society.

[Cites] Haematologica. 2000 Mar;85(3):246-9 [10702811.001]

[Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]

[Cites] J Biol Chem. 1990 Oct 25;265(30):18227-33 [2211699.001]

[Cites] Blood. 1999 Jan 15;93(2):632-42 [9885226.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]

[Cites] Br J Haematol. 2005 Sep;130(5):726-8 [16115128.001]

[Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]

[Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]

[Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]

[Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]

[Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]

[Cites] Leukemia. 2006 Sep;20(9):1644-6 [16791266.001]

[Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]

[Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]

[Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]

[Cites] Leukemia. 2007 Sep;21(9):2052-4; author reply 2054; discussion 2055-6 [17637816.001]

[Cites] Blood. 2008 Feb 15;111(4):1855-61 [18056840.001]

[Cites] Am J Clin Pathol. 2001 Dec;116(6):886-92 [11764078.001]

(PMID = 19637342.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / U54 CA096300

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin

[Other-IDs] NLM/ NIHMS633932; NLM/ PMC4199225

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.

BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).

DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).

RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<M2<M4eo<M4<M0<M1<M5a<M5b.

Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.

On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).

In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency for a worse overall (p=0.059) and event free (p=0.087) survival was found.

[MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

Genetic Alliance. consumer health - Leukemia, Myeloid.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]

(PMID = 16330434.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.

The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor acute myeloid leukemia (AML).

A side effect of administration of G-CSF is an increase in peripheral white blood cell count and blast cell percentage during the recovery phase of the bone marrow after induction chemotherapy.

A 60-year-old man with inversion 16 AML was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.

Our case report underscores the importance of recognizing this phenomenon associated with the administration of G-CSF, and waiting for 5-7 days before administering re-induction therapy or classifying the disease as primary refractory AML.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. VIDARABINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20709669.001).

[ISSN] 2152-2669

[Journal-full-title] Clinical lymphoma, myeloma & leukemia

[ISO-abbreviation] Clin Lymphoma Myeloma Leuk

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration of leukemia cells could be demonstrated.

Bone marrow of leukemia patients shows an increased microvessel density as well as VEGF expression.

Complete remissions in acute myeloid leukemia (AML) have been reported by targeting the receptor tyrosine kinase system of VEGF.

While the pathophysiology behind the contribution of VEGF to leukemia progression is not yet completely understood, VEGF and its receptors may provide promising targets not only in solid tumors but also hematological malignancies such as AML.

[MeSH-minor] Cell Proliferation. Cell Survival. Disease Progression. Humans

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17305503.001).

[ISSN] 1873-5592

[Journal-full-title] Current drug targets

[ISO-abbreviation] Curr Drug Targets

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor

[Number-of-references] 226

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.

[MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Leukemia, Myeloid, Acute / complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. AMPHOTERICIN B .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16961579.001).

[ISSN] 0933-7407

[Journal-full-title] Mycoses

[ISO-abbreviation] Mycoses

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Their response to "missing self" signals was described 3 decades ago, but the recent discovery of a panoply of activating receptors has made it clear that NK cell reactivity arises from a combination of inhibitory and activating signals.

Successful clinical exploitation of NK cell reactivity was demonstrated in allogeneic transplantation for acute myelogenous leukemia from HLA-haploidentical donors when matched donors were not available.

This review summarizes the heterogeneous clinical results and explains them based on a succinct description of NK cell biology.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Eur J Immunol. 2004 Oct;34(10):2699-707 [15368286.001]

[Cites] Nat Immunol. 2004 Oct;5(10):996-1002 [15454923.001]

[Cites] Transplantation. 2004 Oct 15;78(7):1081-5 [15480179.001]

[Cites] Leukemia. 2004 Nov;18(11):1835-8 [15457184.001]

[Cites] N Engl J Med. 1985 Sep 26;313(13):765-71 [3897863.001]

[Cites] Blood. 2005 Nov 15;106(10):3666-72 [16046526.001]

[Cites] Blood. 2005 Dec 15;106(13):4370-6 [16131567.001]

[Cites] J Immunol. 2006 Feb 1;176(3):1517-24 [16424180.001]

[Cites] J Immunol. 2006 Feb 1;176(3):1582-7 [16424187.001]

[Cites] Blood. 2006 Feb 1;107(3):1230-2 [16239436.001]

[Cites] Annu Rev Immunol. 2006;24:257-86 [16551250.001]

[Cites] Cancer Res. 2006 Jun 1;66(11):5927-33 [16740733.001]

[Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):828-36 [16864053.001]

[Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):876-84 [16864058.001]

[Cites] Transplantation. 2006 Oct 27;82(8):1024-30 [17060849.001]

[Cites] Biol Blood Marrow Transplant. 2006 Oct;12(10):1073-84 [17084371.001]

[Cites] Immunol Rev. 2006 Dec;214:155-60 [17100883.001]

[Cites] Blood. 2007 Jan 1;109(1):323-30 [16940427.001]

[Cites] J Clin Oncol. 2007 Feb 20;25(6):690-7 [17228020.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3384-9 [17360655.001]

[Cites] Nat Rev Immunol. 2007 May;7(5):329-39 [17438573.001]

[Cites] Immunity. 2007 Apr;26(4):503-17 [17398124.001]

[Cites] Immunology. 2007 Jun;121(2):258-65 [17346281.001]

[Cites] Blood. 2007 Jun 1;109(11):5058-61 [17317850.001]

[Cites] Immunity. 2007 May;26(5):593-604 [17509909.001]

[Cites] Blood. 2007 Jul 1;110(1):433-40 [17371948.001]

[Cites] J Immunol. 2007 Jul 1;179(1):89-94 [17579025.001]

[Cites] Immunity. 2007 Jun;26(6):798-811 [17540585.001]

[Cites] Science. 2002 May 17;296(5571):1323-6 [11950999.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8826-31 [12060703.001]

[Cites] Blood. 2002 Sep 15;100(6):1935-47 [12200350.001]

[Cites] J Immunol. 2002 Oct 15;169(8):4253-61 [12370356.001]

[Cites] Blood. 2005 May 15;105(10):4135-42 [15687235.001]

[Cites] J Immunol. 2005 May 15;174(10):6540-5 [15879158.001]

[Cites] Tissue Antigens. 2005 Jun;65(6):519-28 [15896199.001]

[Cites] J Clin Oncol. 2005 May 20;23(15):3447-54 [15753458.001]

[Cites] J Immunol. 1999 Nov 15;163(10):5269-77 [10553049.001]

[Cites] J Exp Med. 1999 Nov 15;190(10):1505-16 [10562324.001]

[Cites] J Neuroimmunol. 2000 Jul 24;107(2):220-5 [10854660.001]

[Cites] Bone Marrow Transplant. 2000 Dec;26(12):1281-90 [11223967.001]

[Cites] Immunity. 2001 Feb;14(2):123-33 [11239445.001]

[Cites] Blood. 2001 May 15;97(10):3132-7 [11342440.001]

[Cites] J Immunol. 2001 Aug 15;167(4):2068-73 [11489989.001]

[Cites] Immunogenetics. 2001 May-Jun;53(4):279-87 [11491531.001]

[Cites] Nature. 2001 Sep 13;413(6852):165-71 [11557981.001]

[Cites] J Exp Med. 2002 Feb 4;195(3):327-33 [11828007.001]

[Cites] J Exp Med. 2002 Feb 4;195(3):343-51 [11828009.001]

[Cites] Biol Blood Marrow Transplant. 2002;8(1):17-25 [11846352.001]

[Cites] Science. 2002 Mar 15;295(5562):2029-31 [11896262.001]

[Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]

[Cites] Nature. 2002 Oct 17;419(6908):734-8 [12384702.001]

[Cites] Blood. 2002 Nov 15;100(10):3825-7 [12393440.001]

[Cites] Blood. 2002 Nov 15;100(10):3633-8 [12393617.001]

[Cites] Immunogenetics. 2002 Nov;54(8):543-50 [12439616.001]

[Cites] Immunity. 2003 Jan;18(1):1-6 [12530970.001]

[Cites] J Immunol. 2003 Feb 15;170(4):1763-9 [12574340.001]

[Cites] J Immunol. 2003 Apr 1;170(7):3572-6 [12646619.001]

[Cites] Blood. 2003 Apr 15;101(8):3052-7 [12480696.001]

[Cites] Blood. 2003 May 1;101(9):3730-40 [12511415.001]

[Cites] Blood. 2003 Jun 15;101(12):4887-93 [12586624.001]

[Cites] Blood. 2003 Aug 1;102(3):814-9 [12689936.001]

[Cites] Blood. 2003 Aug 15;102(4):1541-7 [12714500.001]

[Cites] Trends Immunol. 2003 Nov;24(11):603-9 [14596885.001]

[Cites] Biol Blood Marrow Transplant. 2003 Dec;9(12):727-41 [14677112.001]

[Cites] J Immunol. 2004 Jan 1;172(1):644-50 [14688377.001]

[Cites] J Immunol. 2004 Feb 1;172(3):1333-9 [14734707.001]

[Cites] Blood. 2004 Feb 15;103(4):1521-6 [14504099.001]

[Cites] Blood. 2004 Apr 1;103(7):2860-1; author reply 2862 [15033884.001]

[Cites] Blood. 2004 Jul 1;104(1):170-7 [15016654.001]

[Cites] Blood. 2008 Sep 15;112(6):2369-80 [18583565.001]

[Cites] Blood. 2008 Oct 1;112(7):2990-5 [18492955.001]

[Cites] PLoS One. 2008;3(10):e3377 [18852879.001]

[Cites] J Immunol. 2008 Nov 1;181(9):6010-9 [18941190.001]

[Cites] Clin Cancer Res. 2008 Nov 15;14(22):7251-9 [19010841.001]

[Cites] Blood. 2007 Jul 15;110(2):606-15 [17405908.001]

[Cites] Ann N Y Acad Sci. 2007 Jun;1106:279-89 [17442774.001]

[Cites] Blood. 2007 Sep 1;110(5):1530-9 [17495133.001]

[Cites] Leukemia. 2007 Oct;21(10):2145-52 [17673900.001]

[Cites] Biol Blood Marrow Transplant. 2007 Nov;13(11):1249-67 [17950913.001]

[Cites] Blood Cells Mol Dis. 2008 Jan-Feb;40(1):84-90 [17964828.001]

[Cites] J Immunol. 2008 Jan 1;180(1):418-25 [18097043.001]

[Cites] Biol Blood Marrow Transplant. 2008 Jan;14(1):75-87 [18158964.001]

[Cites] Blood. 2008 Feb 1;111(3):1309-17 [17947507.001]

[Cites] Leukemia. 2008 Feb;22(2):249-57 [18046448.001]

[Cites] Immunity. 2008 Apr;28(4):571-80 [18394936.001]

[Cites] Nat Immunol. 2008 May;9(5):486-94 [18425105.001]

[Cites] Nat Immunol. 2008 May;9(5):495-502 [18425106.001]

[Cites] Nat Immunol. 2008 May;9(5):503-10 [18425107.001]

[Cites] J Immunol. 2008 Jun 15;180(12):7785-91 [18523242.001]

[Cites] Blood. 2008 Jul 15;112(2):435-43 [18385451.001]

[Cites] Stem Cells. 2008 Aug;26(8):2114-23 [18535152.001]

[Cites] Immunol Rev. 2008 Aug;224:98-123 [18759923.001]

[Cites] Nature. 1986 Feb 20-26;319(6055):675-8 [3951539.001]

[Cites] J Immunol. 1988 Nov 15;141(10):3478-85 [2903193.001]

[Cites] N Engl J Med. 1989 Jan 26;320(4):197-204 [2643045.001]

[Cites] Immunol Today. 1990 Jul;11(7):237-44 [2201309.001]

[Cites] Haematologica. 2008 Dec;93(12):1852-8 [18945751.001]

[Cites] J Exp Med. 2008 Dec 22;205(13):2959-64 [19029379.001]

[Cites] Blood. 2009 Jan 15;113(3):726-32 [18945962.001]

[Cites] Blood. 2009 Mar 12;113(11):2434-41 [18974374.001]

[Cites] Blood. 2009 Mar 26;113(13):3119-29 [18945967.001]

[Cites] Blood. 2009 May 28;113(22):5628-34 [19329778.001]

[Cites] J Immunol. 2008 Dec 1;181(11):7453-7 [19017932.001]

[Cites] Bone Marrow Transplant. 1991 Jan;7(1):23-33 [2043874.001]

[Cites] Science. 1993 May 21;260(5111):1121-4 [8493555.001]

[Cites] Immunol Cell Biol. 1993 Jun;71 ( Pt 3):201-8 [8349302.001]

[Cites] Blood. 1994 Dec 1;84(11):3948-55 [7524753.001]

[Cites] Int J Radiat Oncol Biol Phys. 1995 Nov 1;33(4):881-6 [7591898.001]

[Cites] Nat Med. 1995 Dec;1(12):1268-73 [7489407.001]

[Cites] J Immunol. 1996 Jun 15;156(12):4746-56 [8648121.001]

[Cites] J Clin Oncol. 1997 May;15(5):1767-77 [9164184.001]

[Cites] J Exp Med. 1997 Oct 6;186(7):1129-36 [9314561.001]

[Cites] Nature. 1998 Feb 19;391(6669):795-9 [9486650.001]

[Cites] J Exp Med. 1998 Jun 15;187(12):2065-72 [9625766.001]

[Cites] N Engl J Med. 1998 Oct 22;339(17):1186-93 [9780338.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14326-31 [9826699.001]

[Cites] Blood. 1999 Jan 15;93(2):467-80 [9885208.001]

[Cites] Blood Cells Mol Dis. 2004 Nov-Dec;33(3):261-6 [15528141.001]

[Cites] Blood Cells Mol Dis. 2004 Nov-Dec;33(3):281-7 [15528145.001]

[Cites] Blood. 2004 Dec 1;104(12):3664-71 [15304389.001]

[Cites] Nat Immunol. 2004 Dec;5(12):1260-5 [15531883.001]

[Cites] J Biol Chem. 2004 Dec 24;279(52):53907-14 [15471859.001]

[Cites] Blood. 2005 Mar 1;105(5):2066-73 [15536144.001]

[Cites] Exp Hematol. 2005 Mar;33(3):344-52 [15730858.001]

[Cites] Blood. 2005 Mar 15;105(6):2594-600 [15536148.001]

[Cites] Trends Immunol. 2005 Apr;26(4):221-6 [15797513.001]

[Cites] Blood. 2005 Apr 15;105(8):3051-7 [15632206.001]

[Cites] Blood. 2005 May 1;105(9):3615-22 [15657183.001]

[Cites] Blood. 2005 Jun 15;105(12):4878-84 [15731175.001]

[Cites] Leukemia. 2005 Aug;19(8):1446-51 [15973456.001]

[Cites] Nature. 2005 Aug 4;436(7051):709-13 [16079848.001]

[Cites] Nat Immunol. 2005 Sep;6(9):938-45 [16086018.001]

[Cites] J Immunol. 2005 Nov 1;175(9):5966-74 [16237090.001]

(PMID = 19539207.001).

[ISSN] 1523-6536

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / R01 CA125276-02; United States / NCI NIH HHS / CA / CA125276-02; United States / NCI NIH HHS / CA / R01 CA125276

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] United States

[Number-of-references] 139

[Other-IDs] NLM/ NIHMS205040; NLM/ PMC2884143

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] RUNX1 DNA-binding mutants, associated with minimally differentiated acute myelogenous leukemia, disrupt myeloid differentiation.

Mutations in the RUNX1 gene are found at high frequencies in minimally differentiated acute myelogenous leukemia.

Significantly, the RDB mutants did not act in a transdominant fashion in vivo to disrupt Runx1 activity in either T-cell or platelet development, which are highly sensitive to Runx1 dosage.

Disruption of the interface that binds CBFbeta, an important cofactor of Runx1, did not impair RDB mutant replating activity, arguing against inactivation of Runx1 function by CBFbeta sequestration.

[MeSH-major] Cell Differentiation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17234761.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / RUNX1 protein, human

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].

OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.

METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.

The cell cycle was examined by flow cytometric analysis.

(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).

CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.

Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.

[MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16029562.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] I kappa B-mediated apoptotic gene therapy against acute myelogenous leukemia using replication-defective HSV-1 vector expressing TK and mutant I kappa B alpha.

Overexpression of NF-kappa B reportedly plays anti-apoptotic roles in the growth of AML cells.

Control of AML cell growth was attempted using a replication-defective herpes simplex virus-1 vector, T0I kappa B alpha, overexpressing mutant I kappa B alpha to inhibit NF-kappa B in vitro.

Infection of T0I kappa B alpha at 15 multiplicity of infection (MOI) with cells of AML lines, HL60, K562, and NB4 displaying >90% infection efficiency and tumor killing in vitro.

Fresh AML cells from 8 patients were infected with T0I kappa B alpha at 3 MOI, with or without GCV or 10 microM of Ara-C in vitro.

Our results suggest that T0I kappa B alpha-mediated gene therapy induces apoptosis of AML cells in vitro.

[MeSH-major] Apoptosis. Genetic Therapy. Herpesvirus 1, Human / genetics. I-kappa B Kinase / metabolism. I-kappa B Proteins / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Genes and Gene Therapy.

Hazardous Substances Data Bank. GANCICLOVIR .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16171566.001).

[ISSN] 1165-158X

[Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)

[ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / I-kappa B Proteins; EC 2.7.1.21 / Thymidine Kinase; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3; P9G3CKZ4P5 / Ganciclovir

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.

To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML).

AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites.

The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival.

Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases.

Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival.

In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response.

These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Exp Hematol. 2006 Oct;34(10):1403-12 [16982333.001]

[Cites] Cancer Immunol Immunother. 2007 Jan;56(1):48-59 [16612596.001]

[Cites] Haematologica. 2007 Jan;92(1):72-80 [17229638.001]

[Cites] Cancer Sci. 2007 Mar;98(3):416-23 [17270031.001]

[Cites] Immunol Res. 2006;36(1-3):73-82 [17337768.001]

[Cites] J Clin Invest. 2004 Nov;114(10):1389-97 [15545986.001]

[Cites] J Clin Invest. 2004 Nov;114(10):1398-403 [15545987.001]

[Cites] Bone Marrow Transplant. 2004 Dec;34(11):923-8 [15361911.001]

[Cites] Blood Rev. 2005 Nov;19(6):289-300 [16275419.001]

[Cites] Eur J Haematol. 2005 Dec;75(6):468-76 [16313258.001]

[Cites] Cancer Immunol Immunother. 2006 Jan;55(1):68-75 [15891884.001]

[Cites] Nature. 2001 Apr 26;410(6832):1107-11 [11323675.001]

[Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]

[Cites] Methods. 2003 Oct;31(2):127-34 [12957570.001]

[Cites] Cancer Res. 2004 Jun 1;64(11):3914-21 [15173002.001]

[Cites] J Allergy Clin Immunol. 2004 Aug;114(2):296-301 [15316506.001]

[Cites] Blood. 1995 Oct 1;86(7):2732-40 [7670112.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] Blood. 1999 Aug 15;94(4):1201-8 [10438707.001]

[Cites] Curr Opin Oncol. 2006 Mar;18(2):107-14 [16462177.001]

[Cites] J Immunol. 2006 Mar 15;176(6):3342-9 [16517701.001]

[Cites] Int J Cancer. 2007 Jun 15;120(12):2723-33 [17315189.001]

[Cites] Cancer Immunol Immunother. 2007 Jul;56(7):943-57 [17180671.001]

[Cites] Blood. 2007 Apr 1;109(7):2871-7 [17164341.001]

[Cites] J Immunol. 2007 Jun 1;178(11):6840-8 [17513732.001]

[Cites] Gastroenterology. 2007 Jun;132(7):2328-39 [17570208.001]

[Cites] Blood. 2007 Jul 1;110(1):409-17 [17374741.001]

[Cites] Cancer Immun. 2007;7:10 [17591743.001]

[Cites] Exp Oncol. 2007 Jun;29(2):102-5 [17704740.001]

[Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5243-8 [17875751.001]

[Cites] J Immunol. 2007 Oct 1;179(7):4919-28 [17878392.001]

[Cites] Blood. 2007 Nov 1;110(9):3480-8 [17606761.001]

[Cites] Blood. 2007 Nov 1;110(9):3192-201 [17616639.001]

[Cites] Cell Death Differ. 2008 Jan;15(1):70-9 [18007660.001]

[Cites] Immunity. 2007 Dec;27(6):985-97 [18082432.001]

[Cites] Cytotherapy. 2007;9(8):755-70 [17917887.001]

[Cites] Int J Cancer. 2008 Apr 15;122(8):1794-802 [18076066.001]

[Cites] Curr Med Chem. 2008;15(10):991-6 [18393856.001]

[Cites] J Immunother. 2008 Feb-Mar;31(2):121-31 [18481382.001]

[Cites] J Immunother. 2008 Feb-Mar;31(2):189-98 [18481388.001]

[Cites] J Immunol. 2008 Sep 1;181(5):3291-300 [18714001.001]

[Cites] J Exp Med. 2008 Sep 1;205(9):2125-38 [18725522.001]

[Cites] Best Pract Res Clin Haematol. 2008 Sep;21(3):455-66 [18790449.001]

[Cites] Biol Blood Marrow Transplant. 2008 Oct;14(10):1088-99 [18804038.001]

[Cites] J Immunother. 2008 Oct;31(8):742-51 [18779745.001]

[Cites] J Exp Med. 2008 Sep 29;205(10):2221-34 [18794336.001]

[Cites] Am J Hematol. 2008 Oct;83(10):771-7 [18756547.001]

[Cites] Int J Immunopathol Pharmacol. 2008 Jul-Sep;21(3):493-500 [18831916.001]

[Cites] Transplantation. 2008 Oct 27;86(8):1125-34 [18946352.001]

[Cites] Expert Opin Biol Ther. 2008 Dec;8(12):1897-920 [18990077.001]

[Cites] J Immunol. 2008 Dec 15;181(12):8209-13 [19050237.001]

[Cites] Scand J Immunol. 2008 Dec;68(6):572-8 [19055696.001]

[Cites] Clin Cancer Res. 2008 Dec 15;14(24):8270-8 [19088044.001]

[Cites] J Clin Oncol. 2009 Jan 10;27(2):186-92 [19064967.001]

[Cites] Blood. 2009 Feb 12;113(7):1581-8 [18974373.001]

[Cites] Clin Cancer Res. 2009 May 15;15(10):3325-32 [19417016.001]

(PMID = 19724059.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin

[Other-IDs] NLM/ PMC2773484

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].

[Transliterated title] Diagnostiek van acute myeloïde leukemie in een stroomversnelling door toepassing van DNA-microarrays.

Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the classification of acute myeloid leukaemia (AML).

In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups of AML.

Chromosomal lesions, mutations, and abnormal gene expression with prognostic value determined the clustering.

In fact, gene-expression profiling recognized leukaemias with certain chromosomal aberrations that had been missed by routine cytogenetics.

Thus, gene-expression profiling allows a comprehensive classification of AML that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.

[MeSH-major] Chromosome Aberrations. Gene Expression Profiling / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Oligonucleotide Array Sequence Analysis

[MeSH-minor] Acute Disease. Cluster Analysis. Cytogenetic Analysis. Humans

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22 [15813427.001]

(PMID = 15813428.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] English Abstract; Journal Article

[Publication-country] Netherlands

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The International Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).

The time until 25% developed acute myeloid leukemia (AML) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).

Only 1 of 20 long-term responders developed AML.

There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk of AML evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.

Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should not be considered candidates for this treatment.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Cell Transformation, Neoplastic. Female. Humans. Leukemia, Myeloid / etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome

Genetic Alliance. consumer health - Anemia.

MedlinePlus Health Information. consumer health - Anemia.

MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15840690.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.

Graft-versus-host disease (GVHD) is a serious complication of allogeneic stem cell transplantation for hematologic diseases.

Polymorphisms are known for FcgammaRIIa, and this molecule is present on endothelial, dendritic, and Langerhans cells.

Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-leukemia (GVL) effect.

Because the FcgammaRIIa molecule is also present on acute myeloid leukemia (AML) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.

We retrospectively studied 73 AML patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.

Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of acute GVHD.

The relapse incidence was not significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk AML patients with the pro-GVL mismatch.

We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for acute GVHD.

[MeSH-major] Antigens, CD / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics

[MeSH-minor] Acute Disease. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs Leukemia Effect / genetics. Graft vs Leukemia Effect / immunology. Humans. Incidence. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous

Genetic Alliance. consumer health - Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15744239.001).

[ISSN] 1083-8791

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.

BACKGROUND: The accurate diagnosis of TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.

Recent studies indicate that a lipoarabinomannan (LAM) assay (Clearview-TB(R)-ELISA) may have some utility for the diagnosis of TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.

The utility of LAM in sputum samples has, hitherto, not been evaluated.

METHODS: LAM was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.

Culture positivity for M. tuberculosis was used as the reference standard for TB diagnosis.

Urine-LAM positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).

Urine-LAM remained highly specific in all 3 subgroups (95%-100%).

25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-LAM.

Sputum-LAM had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.

CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-LAM is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would otherwise have required further investigation.

Genetic Alliance. consumer health - HIV.

MedlinePlus Health Information. consumer health - HIV/AIDS.

MedlinePlus Health Information. consumer health - HIV/AIDS in Women.

MedlinePlus Health Information. consumer health - Tuberculosis.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Microbiol. 2000 Jun;38(6):2278-83 [10834989.001]

[Cites] J Acquir Immune Defic Syndr. 2009 Oct 1;52(2):145-51 [19692904.001]

[Cites] Scand J Infect Dis. 2001;33(4):279-84 [11345220.001]

[Cites] Arch Intern Med. 2003 May 12;163(9):1009-21 [12742798.001]

[Cites] Semin Respir Infect. 2003 Dec;18(4):263-71 [14679475.001]

[Cites] Clin Chem. 2004 Mar;50(3):473-6 [14981027.001]

[Cites] Radiology. 1982 Apr;143(1):29-36 [7063747.001]

[Cites] JAMA. 1982 May 14;247(18):2543-6 [7069920.001]

[Cites] J Immunol Methods. 1996 Apr 19;190(2):151-61 [8621950.001]

[Cites] Trans R Soc Trop Med Hyg. 2005 Dec;99(12):893-900 [16139316.001]

[Cites] Int J Tuberc Lung Dis. 2006 Jan;10(1):31-8 [16466034.001]

[Cites] Expert Rev Mol Diagn. 2006 May;6(3):423-32 [16706744.001]

[Cites] AIDS. 2007 Feb 19;21(4):423-32 [17301560.001]

[Cites] Lancet. 2007 Jun 16;369(9578):2042-9 [17574096.001]

[Cites] PLoS One. 2009;4(3):e4689 [19277111.001]

[Cites] Curr Opin Pulm Med. 2009 May;15(3):188-200 [19387262.001]

[Cites] J Clin Invest. 2009 May;119(5):1085-9 [19422099.001]

[Cites] Int J Tuberc Lung Dis. 2009 Aug;13(8):989-95 [19723379.001]

[Cites] BMC Infect Dis. 2009;9:141 [19715562.001]

[Cites] Int J Tuberc Lung Dis. 2009 Oct;13(10):1253-9 [19793430.001]

[Cites] Clin Chest Med. 2009 Dec;30(4):701-16, viii [19925962.001]

[Cites] AIDS. 2009 Sep 10;23(14):1875-80 [20108382.001]

[Cites] J Microbiol Methods. 2001 May;45(1):41-52 [11295196.001]

(PMID = 20352098.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] ENG

[Grant] None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2844421

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Core binding factor acute myeloid leukemia.

Core binding factor (CBF) acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult de novo AML cases.

Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16) AML, thereby supporting the notion that they represent two distinct biologic and clinical entities.

Furthermore, despite being considered as a more favorable AML risk group, only approximately half of the CBF AML patients are cured with current therapy, indicating the need for improved therapeutic approaches.

This review summarizes the most recent laboratory and clinical discoveries relevant to this subset of AML and how they are being applied for in an effort to improve the cure rate in patients with the disease.

[MeSH-major] Chromosome Inversion. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Translocation, Genetic

[MeSH-minor] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual / diagnosis. Prognosis

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18692691.001).

[ISSN] 0093-7754

[Journal-full-title] Seminars in oncology

[ISO-abbreviation] Semin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors

[Number-of-references] 76

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.

BACKGROUND: Therapy-related myeloid neoplasm (t-MN) is a distinct class of acute myeloid leukemia (AML) in the World Health Organization (WHO) classification.

Both AML and acute lymphoblastic leukemia (ALL) may develop after treatment for primary cancer.

Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related acute leukemias (t-AL).

METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed acute leukemia.

Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related AML (t-AML) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 2003 Apr 1;21(7):1195-204 [12663705.001]

[Cites] Semin Hematol. 1996 Jul;33(3):256-73 [8819235.001]

[Cites] J Clin Oncol. 2005 Jun 20;23(18):4179-91 [15961765.001]

[Cites] Zentralbl Gynakol. 2005 Aug;127(4):235-41 [16037905.001]

[Cites] Br J Haematol. 2007 Feb;136(4):590-6 [17367411.001]

[Cites] Br J Haematol. 2007 Jun;137(6):513-29 [17539774.001]

[Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]

[Cites] Haematologica. 2007 Oct;92(10):1389-98 [17768113.001]

[Cites] Leuk Lymphoma. 2008 Feb;49(2):204-17 [18231906.001]

[Cites] Cancer Res. 2008 Dec 15;68(24):10024-7 [19074864.001]

[Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]

[Cites] Breast Cancer Res Treat. 2009 Dec;118(3):593-8 [19322652.001]

[Cites] Am J Clin Pathol. 2010 Jan;133(1):75-82 [20023261.001]

[Cites] Am J Med Sci. 2010 Jan;339(1):36-40 [19996729.001]

[Cites] Chem Biol Interact. 2010 Mar 19;184(1-2):39-45 [20026017.001]

[Cites] Korean J Lab Med. 2010 Jun;30(3):255-9 [20603585.001]

[Cites] Cancer. 2004 Oct 1;101(7):1529-36 [15378478.001]

[Cites] Br J Haematol. 1999 Sep;106(4):1037-40 [10520009.001]

(PMID = 21120206.001).

[ISSN] 2092-9129

[Journal-full-title] The Korean journal of hematology

[ISO-abbreviation] Korean J Hematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2983048

[Keywords] NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Body weight, 10th rib backfat (BF10), last rib backfat (LRF), and loin muscle area (LMA) were serially measured at 10, 13, 16, 19, 22, 24, and 26 wk of age.

At 26 wk of age, Duroc-sired progeny were heavier (143.4 vs. 132.7 kg, P < 0.001), had more BF10 (27.1 vs. 23.7 mm, P < 0.001) and LRF (21.2 vs. 19.2 mm, P < 0.001), but had similar LMA (46.4 vs. 47.1 cm2) compared with Pietrain-sired progeny.

Mean feed efficiency did not differ between breed of sire in any period of the study.

Random regression animal models with polynomial regression on week on-test were fitted to BW, BF10, LRF, LMA, FFTOLN, TOFAT, EBPRO, and EBLIPID from 10 to 26 wk of age.

Serial heritability estimates generally increased from 10 to 26 wk of age with ranges as follows: BW (0.05 to 0.39), BF10 (0.13 to 0.76), LRF (0.11 to 0.79), LMA (0.05 to 0.73), FFTOLN (0.07 to 0.16), TOFAT (0.19 to 0.45), EBPRO (0.02 to 0.55), and EBLIPID (0.12 to 0.60).

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16424252.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mucormycosis resulting in gastric perforation in a patient with acute myelogenous leukemia: report of a case.

Mucormycosis is an uncommon opportunistic fungal infection that may develop in immunocompromised patients with conditions such as diabetes mellitus, leukemia, lymphoma, or human immunodeficiency virus (HIV), or after transplantation with immunosupperessive therapy.

We report a case of gastric perforation caused by a mucormycosis infection in a patient with acute myelogenous leukemia (AML).

[MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Gastrectomy. Intestinal Perforation / etiology. Leukemia, Myeloid, Acute / drug therapy. Mucormycosis / complications. Stomach / injuries. Treatment Outcome

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

Hazardous Substances Data Bank. AMPHOTERICIN B .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Gastroenterol. 1979 Oct;72 (4):379-94 [517498.001]

[Cites] Surg Today. 2003;33(4):319-22 [12707834.001]

[Cites] Gastroenterology. 1969 Nov;57(5):579-86 [4981541.001]

[Cites] Br J Surg. 1974 Sep;61(9):743-6 [4413541.001]

[Cites] Am J Gastroenterol. 1999 Jan;94(1):252-6 [9934766.001]

[Cites] Clin Infect Dis. 2003 Jul 15;37(2):221-9 [12856215.001]

[Cites] Arch Intern Med. 1995 May 22;155(10):1093-8 [7748054.001]

[Cites] Clin Microbiol Rev. 2000 Apr;13(2):236-301 [10756000.001]

[Cites] Pharmacotherapy. 2002 Apr;22(4):519-26 [11939688.001]

[Cites] Haematologica. 2004 Feb;89(2):207-14 [15003897.001]

[Cites] Ann Hematol. 2003 Oct;82 Suppl 2:S133-40 [13680170.001]

[Cites] Pediatr Pulmonol. 1997 Mar;23(3):222-5 [9094732.001]

[Cites] Am J Gastroenterol. 1998 Aug;93(8):1360-2 [9707066.001]

[Cites] Rev Infect Dis. 1989 Sep-Oct;11(5):741-54 [2682947.001]

[Cites] Antimicrob Agents Chemother. 1997 Jun;41(6):1275-80 [9174183.001]

[Cites] Arch Intern Med. 1978 Jun;138(6):925-7 [646564.001]

[Cites] Medicine (Baltimore). 1986 Mar;65(2):113-23 [3951358.001]

[Cites] Drugs. 2004;64(18):1997-2020 [15341494.001]

(PMID = 16937290.001).

[ISSN] 0941-1291

[Journal-full-title] Surgery today

[ISO-abbreviation] Surg. Today

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B